Our first exposure to Phencyclidine occurred during the summer of 1967 in the Haight-Ashbury District of San Francisco in which the drug was first introduced as the “PeaCe Pill” during a rock concert. We saw that day between twenty-five and thirty acute Phencyclidine toxic reactions. In some respects, these reactions were like the bad LSD trips we were used to treating, but in other respects quite different, with greater physical toxicity and paranoid thinking. We had samples of the “PeaCe Pill” analyzed through a local Bay Area toxicology laboratory and found that the psychoactive drug was PCP. The “PeaCe Pill” was not well received by the majority of individuals in Haight-Ashbury at that time, although Phencyclidine became the drug of choice for a small number of users who continued to use it on a chronic basis. For them most part, Phencyclidine was a drug of deception, usually marketed as “THC” or as one of the psychedelics which were more in demand. Within the past five years, however, Phencyclidine has become increasingly visible as a primary drug of abuse under a variety of street names, including “hog,” “krystal,” and “angel’s dust.” The drug is illicitly manufactured and taken in a variety of ways: orally, intranasally, and by intramuscular or intravenous injection. This paper provides the clinician who treats Phencyclidine problem with a conceptual framework for the diagnosis and treatment of the Phencyclidine abuse syndrome. Certainly not everybody who uses Phencyclidine develops toxic consequences, but we have seen a variety of short term and long term adverse reactions and have found that many clinicians have difficulty in both the diagnosis and treatment of PCP-induced problems. (Our work is based primarily on the following clinical experience: 1) the Haight-Ashbury Free Medical Clinic Drug Detoxification and Aftercare Program; 2) our Emergency Medical Service at rock concerts; 3) Patient consultation through our Physician Training and Consultation gram, in which we receive telephone calls and individual requests from physicians treating people who have Phencyclidine abuse problems; 4) Outreach Training and Clinical Work: 5) Inpatient treatment of Phencyclidine abusers at Gladman Psychiatric Hospital: 6) our collective private practices; 7) work and patient consultation with other community based treatment agencies; and 8) fellow clinical investigators. Our information is based on our clinical experience and review of literature. There are many more questions than there are answers, and the clinical staging presented later in this paper is designed primarily for the clinician, not the Phencyclidine researcher. As the Phencyclidine abuse problem has increased, clinicians all over the country are faced with management of various stages of Phencyclidine abuse with relatively little help on diagnosis and treatment.

The effects observed when Phencyclidine is ingested result from a complex interaction among pharmacological, physical, and sociocultural variables, and the pre-PCP psychological makeup of the individual. In the natural setting, of course, these variables cannot be isolated. In designing the diagnostic and treatment plan, one is confronted with their simultaneous interaction.

Our clinical findings show four behavioral phases of the Phencyclidine abuse syndrome, which may appear as successive stages.

Stage I. Acute Phencyclidine toxicity: These reactions are a direct result of Phencyclidine intoxication. Their onset may be minutes to hours following Phencyclidine ingestion.

Stage II. Phencyclidine toxic psychosis: This stage is apparently not related to toxic blood levels of Phencyclidine and does not inevitably follow stage I.

Stage III. PCP-precipitated psychotic episodes: In some individuals, Phencyclidine may precipitate a psychotic reaction lasting a month or more which clinically appears much like schizophrenia.

Stage IV. PCP-induced depression: Phencyclidine can produce a depressive reaction in some individuals. This may follow any of the previous stages and last from one day to several months.

Each stage is shown in outline in table 1 and will be described in more detail, followed by case histories illustrating salient clinical features.

Discussion and Case Histories

Stage II. Phencyclidine Toxic Psychosis

After the acute Phencyclidine toxicity phase has passed, some individuals develop a prolonged toxic psychosis. Our experience has been that incidence of the Phencyclidine toxic psychosis is highest among chronic abusers. In trying to detemine prognostic indicators to why certain patients will become psychotic, we have looked at different clinical variables, but found chronic abuse to be the major factor. In this stage, one finds impaired judgment and paranoid delusions with agitation and both auditory and visual hallucinations. The individual can be self-destructive or destructive to others. Hallucinations and flattened affect are characteristic. The usual duration is 24 hours to 7 days or more. Lab results indicate blood negative and urine positive for PCP. The amount of Phencyclidine excreted in the urine is highly dependent upon urinary acidity, and an attempt to collect the urine under conditions of urinary acidification with ammonium chloride or ascorbic acid (vitamin C) should be made.

Phencyclidine Toxic Psychosis: Case 2

A 38-year-old black male with no previous history of drug abuse or psychiatric problem acquired some new marihuana which was described to him as “superweed.” He had regularly smoked marihuana for over twenty years and described no adverse consequences of any sort with its use. He began smoking this new “superweed” and found himself (according to his girlfriend) beaming paranoid, delusional, and uncharacteristically hostile. After approximately two weeks of daily smoking of the “superweed” he felt that there might be some correlation between this new drug and his symptoms and stopped smoking the drug for a day. He found no symptom relief; after that, he actually increased the dosage, as he felt it might help him feel better and recover from the symptoms which he felt were unrelated to the drug use. Shortly after, he became quite assaultive, cut off the head of his dog, and assaulted a stranger on the street with a razor. His girlfriend, who had read in the newspaper of the bizarre behavior Phencyclidine can produce, brought him to the Haight-Ashbury Free Medical Clinic where he was examined. The material was analyzed and found to be marihuana laced with a significant quantity of PCP. The toxicity of Phencyclidine was explained to both the patient and his girlfriend. Both decided on an abrupt cessation of the drug. Following a brief period of hospitalization in which antipsychotic medication was administered, the patient was discharged and refused further hospitalization or medication, but remained in supportive counseling. After approximately two weeks the psychotic symptomatology faded, but the patient still complained of impaired thinking, difficulty in believing that the delusions that he perceived during his Phencyclidine intoxication were unreal, and prolonged depression. Weekly supportive counseling without medication gradually resolved these symptoms in approximately twelve weeks.

Treatment of Stage II

Most clinicians recommend the use of non-phenothiazine tranquilizers such as haloperidol (Haldol). Some clinicians use sedative hypnotic medication. There is no sound research basis for the use of either of these medications; nor in our experience, is there any indication that these medications shorten the course of acute Phencyclidine toxic psychosis. It does appear, however, that they make the patient more manageable in a ward, which is probably the major reason that these medications are used. In those clinical cases that we have seen where patients have received either no medication, sedative hypnotic medication, or antipsychotic medication, these variables do not appear to change the total length of time the individual is psychotic, but they do modify the characteristic symptoms.

Stage III. PCP-precipitated psychotic episode

Early investigators reported on the tendency of Phencyclidine to exaggerate signs and symptoms in schizophrenic patients (). Many other studies have described the PCP-induced psychosis. Luisada and Brown (1976) have described individuals who were not previously schizophrenic, who became so following ingestion of PCP, and who periodically have return of symptoms, although of less intense nature than when the Phencyclidine was first used. To what extent it is possible to have a prolonged psychosis in an individual who is not predisposed to schizophrenia is not known. Certain individuals, mostly with psychotic or prepsychotic personalities, tend to develop a PCP-precipitated psychotic episode that mimics schizophrenia. This may occur after a single dose administration of PCP. This is not a result of chronic Phencyclidine abuse producing a toxic psychosis, but rather a PCP-precipitated adverse reaction to an underlying psychological condition. The characteristics of the episode are of the schizoaffective type with paranoid features and a waxing and waning thought disorder, A majority of the cases that we have seen in stage III have had psychotic or prepsychotic personalities, and we believe that this is the major prognostic indicator. However, we have seen a few cases that have had a prolonged PCP-precipitated psychotic episode after single dose administration, with no unequivocal history of preexisting psychosis. Our time range is 7 days to 30 days or more, with patients moving from the Phencyclidine toxic psychosis into the PCP-precipitated psychotic episode. Lab results indicate blood negative, urine negative. Most investigators recommend the use of chlorpromazine (Thorazine) in dosages comparable to those used in schizophrenia and remark that the paranoia appears to yield at a slower rate (). The need for long term antipsychotic drug maintenance for the individual with PCP-precipitated psychotic episodes makes it important to differentiate the PCP-induced toxic psychosis from the PCP-precipitated psychosis. It is also important to emphasize that individuals with schizophrenia can go into a prolonged psychotic phase after a single dose of PCP. This is demonstrated by the following case:

PCP-precipitated psychotic episode: Case 3

A 26-year-old white female with a long history of psychiatric disturbance, including hospitalization for psychosis, but no history of alcohol or drug abuse, was at a party and shared a joint of “angel dust,” a drug with which she had no previous experience. After smoking approximately half of the joint, she started becoming quite paranoid and delusional, and developed both auditory and visual hallucinations. After remaining at home with her parents for two days, she was taken to a San Francisco psychiatric hospital where she was admitted. The material she smoked was analyzed and found to contain PCP. At the time of hospitalization, both her blood and urine were negative for PCP. She remained psychotic for over two weeks, but the thought disorder gradually faded, giving way to a substantial depression. Her psychosis was treated with haloperidol (Haldol).

Treatment of Stage III

A. Immediate goals of treatment are the same as those described for acute Phencyclidine toxicity, including prevention of injury and reduction of stimuli.

During the PCP-related psychotic break, it appears that the drug precipitates an underlying thought disorder, rather than producing a direct toxic psychosis, which we define as a major break with reality secondary to an intoxicant. In general, many clinicians use a non-phenothiazine major traquilizer, such as haloperidol (Haldol), for the Phencyclidine toxic psychosis because of the concern over the additive effect between Phencyclidine arid chlorpromazine (Thorazine). However, there is no controlled research in humans to support this. Domino and Luby (1972) have described animal research which shows some additive effect of chlorpromazine (Thorazine) and PCP. In PCP-precipitated psychosis, however, experienced clinicians () recommend residential seclusion with frequent observation and high doses of antipsychotic phenothiazine medication, such as chlorpromazine (Thorazine) given daily, starting with 400 mg a day in divided doses and increased as necessary by 200 mg a day to an average daily dose of 1600 mg per day. Clinical experience in the San Francisco Bay Area has varied between the use of sedative hypnotic medication such as diazepam (Valium) and low doses of haloperidol (Haldol) and has avoided the high doses of chlorpromazine (Thorazine) as described by Luisada and Reddick (1978). All clinicians treating stage III, however, agree that the PCP-induced psychotic reaction can be quite prolonged and should be managed on an in-patient basis.

Summary and Questions for Future Research

PCP abuse may present in a variety of ways to the clinician. Treatment strategies may be conceptualized in terms of four stages, each having specific types of treatment intervention: acute Phencyclidine toxicity: Phencyclidine toxic psychosis; PCP-precipitated psychosis; and PCP-induced depression. Clinical treatment of the severe overdose in coma is best understood and defined by clinical protocol. The treatment of other stages is still primarily dictated by clinical intuition; disagreement exists among experienced clinicians as to what constitutes the most appropriate treatment.

For the clinician responsible for treating Phencyclidine abuse, a number of Clinically important questions remain unanswered. For example:

1. Does chronic Phencyclidine use produce long-lasting, perhaps permanent, brain damage? Is the association observed by clinicians spurious in that most Phencyclidine users have used a variety of other drugs? Are the effects thought to be long term actually secondary to chronic intoxication?

2. Does Phencyclidine ingestion produce long-lasting psychological disorganization in individuals who are not schizophrenic? If so, how can these effects be characterized and distinguished from schizophrenia?

3. Are the antipsychotics useful in shortening the duration or intensity of Phencyclidine acute toxicity, the Phencyclidine toxic psychosis, or the PCP-precipitated psychosis? Should patients who manifest prolonged psychoses following Phencyclidine ingestion be diagnosed or treated differently than schizophrenics?

4. Is the PCP-induced depression observed in Phencyclidine users actually induced by the drug? If so, what is the underlying biochemical mechanism, and should the antidepressants be used in treatment of the depression?

The answers to these and other clinically relevant questions can be resolved by careful clinical research. In view of the current differing opinions as treatment, double blind random treatment assignment studies should be undertaken. Practically, the barriers to definitive research include the difficulty in establishing informed consent to participate in a study while the patient is acutely psychotic and the difficulties inherent funding such research. Until answers are available, prudent clinical treatment must proceed according to clinical intuition. We believe the concept of distinct clinical stages is a step toward rational treatment.

Selections from the book: “Phencyclidine (PCP) Abuse: An Appraisal”. Robert C. Petersen, Ph.D., and Richard C. Stillman, M.D., editors. Monograph derived from a technical review to assess state-of-knowledge about phencyclidine and its abuse, and to present areas for additional research.National Institute on Drug Abuse Research Monograph 21, August 1978.